CHOLINERGIC AND ADRENERGIC COMPONENTS IN THE NEUROHUMORAL CONTROL OF THE RELEASE OF LH IN THE RABBIT

Abstract

Earlier work has demonstrated that an adrenergic mediator is involved in the neuro-genic control of the release of luteinizing hormone from the rabbit hypophysis. Ovulation, which signifies the release of luteinizing hormone, was induced by instilling adrenaline, but not acetyl-choline, directly into the anterior hypophysis, and copulation-induced ovulation was blocked by the rapid post-coital injn. of the adrenolytic drug Dibenamine. Like Dibenamine, atropine sulfate (30 mg./kg. intraven.), when injected very quickly after copulation (total dose within a few sec.), blocks ovulation (9 of 13 rabbits failed to ovulate), but not when injn. is delayed 5 min. (11/12 ovulated). However, to be equally effective, atropine must be given earlier than Dibenamine: when injn. was started 15 sec. after the termination of copulation, atropine blocked ovulation in only 3/20 cases while Dibenamine blocked it in 10/13. Thus, a cholinergic (atropine-blocked) component of the copulation-initiated neurogenic stimulus appears to precede the well-established adrenergic component. The natural neurogenic stimulus at copulation traverses the pituitary stalk and the final pathway, distal to the median eminence, is probably the hypophyseal portal system. Possibly in this system, as in the adrenal medulla and sympathetic ganglia, the cholinergic component stimulates the secretion of the adrenergic mediator, which in turn stimulates the hypophyseal cells to release luteinizing hormone. The ovarian follicles whose rupture has been blocked by atropine or Dibenamine almost invariably give histological evidence of partial activation. This includes characteristic preovulatory changes and also an atypical atresia of large follicles, in which the ova precede the granulosa in degeneration. After a follicle has ruptured, the normal development and function of the corpus luteum does not appear to be affected by atropine or Dibenamine.